There are no known effective treatments for Burkholderia cenocepacia (B. cenocepacia or Bc) infections in patients with cystic fibrosis (CF) due to extensive multi-drug resistance (antibiotic resistance) of the bacteria and decreased ability of the immune cells of patients with CF to kill the bacteria. We have demonstrated that defective bacterial killing in patients with CF is caused, in part, by deficient autophagy in immune effector cells such as macrophages. B. cenocepacia is the most problematic and feared pathogenic organism in patients with CF, causing Cepacia syndrome, sepsis, and rapid spread of the bacteria in the infected patient.
Currently, no effective treatments are available for the treatment of B. cenocepacia infections in patients with CF due in part to the resistance to multiple antibiotics by the bacteria. B. cenocepacia infection in CF is a contraindication to life-sustaining lung transplant due to poor survival of infected patients. Immunocompromised patients (e.g., chronic granulomatous disease, ICU patients) are also susceptible to Burkholderia infections. Recent Burkholderia outbreaks in non-CF populations have been extremely virulent. Overall, one in four patients with Burkholderia infections die, and one out of every three patients infected with Burkholderia in the ICU setting die. Hanulik et al., An outbreak of Burkholderia multivorans beyond cystic fibrosis patients. J Hosp Infect. 2013 July; 84(3):248-51. PMID: 23706672.
Available treatments for Pseudomonas aeruginosa are limited due to acquired antibiotic resistance (e.g., hospital-acquired infections). P. aeurginosa infections are common in patients with CF and can cause chronic, persistent infections with long-term morbidity and mortality. In addition, P. aeruginosa multi-drug resistance develops over time with continued antibiotic exposure, as the antibiotic treatment intended to clear the chronic P. aeruginosa infection contributes to the development of antibiotic resistance.
P. aeruginosa infections can be treated by a variety of antibiotics including aminoglycosides, fluoroquinolones, and advanced generation cephalosporins, but treatment with these antibiotics drugs has led to further and extensive drug resistance by the bacteria.
Previously, the celecoxib derived chemical agent AR-12 (a.k.a. OSU-03012), which is an analogue of AR-13, exhibited antibacterial activity against the intracellular bacteria Salmonella Typhimurium and Francisella tularensis in macrophages. AR-12 is an orally bioavailable small molecule with substantial anti-bacterial activity across multiple bacterial pathogens including, for example, Salmonella and Francisella. 
AR-12 is a celecoxib derivative that was discovered at The Ohio State University. The compound was initially developed in the oncology setting and a phase I study demonstrated an acceptable safety profile with long term oral exposures up to 33 weeks. The AR-12 oncology dose most likely substantially exceeds the exposure needed in the infectious disease setting. AR-12 has been previously shown to exhibit anti-tumor and anti-bacterial activity. It is thought that AR-12 induces autophagy of cells harboring intracellular bacteria. Supportive preclinical studies demonstrated that AR-12 has rapid blood brain barrier penetration and appreciable accumulation in tissues, exceeding the blood level concentrations by several fold. Booth L, Roberts J L, Tavallai M, Nourbakhsh A, Chuckalovcak J, Carter J, Poklepovic A, Dent P. OSU-03012 and Viagra Treatment Inhibits the Activity of Multiple Chaperone Proteins and Disrupts the Blood-Brain Barrier: Implications for Anti-Cancer Therapies. J Cell Physiol. 2015 August; 230(8):1982-98. doi: 10.1002/jcp.24977. PubMed PMID: 25736380.
AR-13, an AR-12 analog, has also been shown to have antibacterial activity. See e.g., U.S. Patent Application Publication 2013/0289004.